The goal the project has been to prevent or slow development of cataracts and retinal degeneration. Whether apoptosis or necrosis is the mechanism involved in the Royal College of Surgeons rat retinal dystrophy and associated cataracts is highly significant from the viewpoint of prevention. Apoptosis occurs in less severely damaging conditions than necrosis and follows a specific program of cell death that might be modifiable. In dim cyclic light (1-50 lux), retinal degeneration occurs by apoptosis, detectable at 25 postnatal (pn) days and completed by 60 pn days. Under these conditions, in rats fed a standard NIH-07 diet, cataracts occurred unilaterally by five months and by one year five percent of rats had bilateral mature cataracts (MC's). The incidence of cataracts and retinal degeneration is also highly sensitive to environmental lightning. Rats reared from birth in darkness, where retinal degeneration does not occur, develop no cataracts. Also, rats reared from birth (before development of photoreceptors) in 270 lux (constant light) developed posterior subcapsular cataracts, but no MC's; however, if constant light began at 20-30 pn days, after retinal rod outer segment (ROS) had developed, 70% of rats developed MC's (70% bilateral). In RCS dystrophic rats, antioxidant diets begun at birth (cyclic lighting of 10-40 lux) totally prevented the cataracts but only delayed the retinal degeneration. Dark rearing, however, prevented both. These findings support the hypothesis of cataractogenesis by peroxidized retina lipids of ROS, damaged by retinaldehyde-generated singlet oxygen. In apoptosis, reactive oxygen may be involved, and Bcl-2, which can prevent cell death, is thought to act in a pathway that quenches reactive oxygen molecules.